INTRODUCTION: Traumatic experiences in childhood and maternal separation (MS) in rodents disrupts proper development of the brain including dopaminergic (DA) mesocorticolimbic pathways originating from ventral tegmental area (VTA). Importantly, early‑life stress predisposes for neuropsychiatric disorders and addiction in adulthood. Moreover, MS stress increases the number of VTA tyrosine hydroxylase (TH) immunoreactive DA neurons, raises baseline dopamine levels, and increases its release in response to acute stress in adult rats. However, neuronal mechanisms of these changes have not been fully explored. AIM(S): The current study aimed at determining the influence of MS on VTA DA cells electrophysiology and responsiveness to acute stress at the level of c-fos expression. METHOD(S): Female rats were submitted to MS during PND 2‑14, 3 h daily. In adulthood, some of the rats were subjected to restraint stress and subsequently perfused. The VTA region was cut, stained against TH and c-fos, and double stained neurons were counted. Remaining animals were sacrificed and brain slices containing VTA were prepared for electrophysiological patch‑clamp experiments. Recorded biocytin‑filled cells were stained and assessed as TH+ or TH‑. RESULTS: Our data show that exposure to early life stress leads to a significant reduction of the rheobase and an increased number of action potentials generated vs. injected current – indices of neuronal excitability. Importantly, it was altered in both TH+ and TH‑ VTA neurons. MS combined with restraint stress significantly increased the number of dorsal but not ventral VTA TH+/c‑fos+ cells. CONCLUSIONS: Observed changes in excitability of VTA DA neurons may constitute a neuronal mechanism of the reported elevated dopamine release after MS. Our data indicate that MS alters reactivity of dorsal but not ventral VTA cells to acute stress, which suggests a greater raise in stress-induced DA release in structures innervated by the dorsal VTA. FINANCIAL SUPPORT: Funding: NSC-Poland UMO- ‑2016/21/B/NZ4/00204.
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